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Article: Involvement of protein kinase C and E2F-5 in euxanthone-induced neurite differentiation of neuroblastoma

TitleInvolvement of protein kinase C and E2F-5 in euxanthone-induced neurite differentiation of neuroblastoma
Authors
KeywordsDifferentiation
E2F-5 transcription factor
Euxanthone
Neurite outgrowth
Neuroblastoma
Issue Date2006
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/biocel
Citation
International Journal Of Biochemistry And Cell Biology, 2006, v. 38 n. 8, p. 1393-1401 How to Cite?
AbstractEuxanthone, a neuritogenic agent isolated from the medicinal herb Polygala caudata, has been shown to induce morphological differentiation and neurite outgrowth in murine neuroblastoma Neuro 2a cells (BU-1 subclone). In order to elucidate the underlying mechanisms of euxanthone-induced neurite outgrowth, a proteomic approach was employed. In the present study, two dimensional (2-D) gel electrophoresis and matrix-assisted laser desorption/ionization-time of flight (MALDI-ToF) mass spectrometry were performed to investigate the alterations in protein expression profile of euxanthone-treated BU-1 cells. Fourteen identified proteins were changed in expression levels after induction of neurite growth. These proteins included participants in transcription and cell cycle regulation, calcium influx and calcium signaling, fatty acid metabolism, cytoskeleton reorganization, casein kinase signal transduction, putative transbilayer amphipath transport and protein biosynthesis. Among the 14 identified proteins, E2F transcription factor 5 (E2F-5) was significantly up-regulated after euxanthone treatment. Go6976, a protein kinase C (PKC) α/βI inhibitor, was found to inhibit neuritogenesis and expression of E2F-5 in the euxanthone-treated BU-1 cells, while SH-6, the Akt/PKB inhibitor, had no inhibitory effect. The gene silencing of E2F-5 by small interfering RNA (siRNA) was found to abolish the euxanthone-induced neurite outgrowth. In conclusion, these results indicated that the transcription factor E2F-5 was actively involved in the regulation of euxanthone-induced neurite outgrowth via PKC pathway. © 2006 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/169846
ISSN
2015 Impact Factor: 3.905
2015 SCImago Journal Rankings: 2.003
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHa, WYen_HK
dc.contributor.authorWu, PKen_HK
dc.contributor.authorKok, TWen_HK
dc.contributor.authorLeung, KWen_HK
dc.contributor.authorMak, NKen_HK
dc.contributor.authorYue, PYKen_HK
dc.contributor.authorNgai, SMen_HK
dc.contributor.authorTsai, SNen_HK
dc.contributor.authorWong, RNSen_HK
dc.date.accessioned2012-10-25T04:57:01Z-
dc.date.available2012-10-25T04:57:01Z-
dc.date.issued2006en_HK
dc.identifier.citationInternational Journal Of Biochemistry And Cell Biology, 2006, v. 38 n. 8, p. 1393-1401en_HK
dc.identifier.issn1357-2725en_HK
dc.identifier.urihttp://hdl.handle.net/10722/169846-
dc.description.abstractEuxanthone, a neuritogenic agent isolated from the medicinal herb Polygala caudata, has been shown to induce morphological differentiation and neurite outgrowth in murine neuroblastoma Neuro 2a cells (BU-1 subclone). In order to elucidate the underlying mechanisms of euxanthone-induced neurite outgrowth, a proteomic approach was employed. In the present study, two dimensional (2-D) gel electrophoresis and matrix-assisted laser desorption/ionization-time of flight (MALDI-ToF) mass spectrometry were performed to investigate the alterations in protein expression profile of euxanthone-treated BU-1 cells. Fourteen identified proteins were changed in expression levels after induction of neurite growth. These proteins included participants in transcription and cell cycle regulation, calcium influx and calcium signaling, fatty acid metabolism, cytoskeleton reorganization, casein kinase signal transduction, putative transbilayer amphipath transport and protein biosynthesis. Among the 14 identified proteins, E2F transcription factor 5 (E2F-5) was significantly up-regulated after euxanthone treatment. Go6976, a protein kinase C (PKC) α/βI inhibitor, was found to inhibit neuritogenesis and expression of E2F-5 in the euxanthone-treated BU-1 cells, while SH-6, the Akt/PKB inhibitor, had no inhibitory effect. The gene silencing of E2F-5 by small interfering RNA (siRNA) was found to abolish the euxanthone-induced neurite outgrowth. In conclusion, these results indicated that the transcription factor E2F-5 was actively involved in the regulation of euxanthone-induced neurite outgrowth via PKC pathway. © 2006 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/biocelen_HK
dc.relation.ispartofInternational Journal of Biochemistry and Cell Biologyen_HK
dc.subjectDifferentiationen_HK
dc.subjectE2F-5 transcription factoren_HK
dc.subjectEuxanthoneen_HK
dc.subjectNeurite outgrowthen_HK
dc.subjectNeuroblastomaen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshCarbazoles - Pharmacologyen_US
dc.subject.meshCell Differentiation - Drug Effectsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshE2f Transcription Factors - Genetics - Metabolismen_US
dc.subject.meshElectrophoresis, Gel, Two-Dimensionalen_US
dc.subject.meshGene Silencingen_US
dc.subject.meshIndoles - Pharmacologyen_US
dc.subject.meshNeurites - Drug Effects - Metabolismen_US
dc.subject.meshNeuroblastoma - Metabolism - Pathologyen_US
dc.subject.meshProtein Kinase C - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshProtein Kinase Inhibitors - Pharmacologyen_US
dc.subject.meshProteomics - Methodsen_US
dc.subject.meshProto-Oncogene Proteins C-Akt - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshSpectrometry, Mass, Matrix-Assisted Laser Desorption-Ionizationen_US
dc.subject.meshXanthones - Pharmacologyen_US
dc.titleInvolvement of protein kinase C and E2F-5 in euxanthone-induced neurite differentiation of neuroblastomaen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, KW: kwleung1@hku.hken_HK
dc.identifier.authorityLeung, KW=rp01674en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.biocel.2006.02.002en_HK
dc.identifier.pmid16546434-
dc.identifier.scopuseid_2-s2.0-33646192904en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33646192904&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume38en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1393en_HK
dc.identifier.epage1401en_HK
dc.identifier.isiWOS:000238822600016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridHa, WY=7006802337en_HK
dc.identifier.scopusauthoridWu, PK=14039819200en_HK
dc.identifier.scopusauthoridKok, TW=8675114000en_HK
dc.identifier.scopusauthoridLeung, KW=13106059300en_HK
dc.identifier.scopusauthoridMak, NK=35587830100en_HK
dc.identifier.scopusauthoridYue, PYK=8570616200en_HK
dc.identifier.scopusauthoridNgai, SM=7006074219en_HK
dc.identifier.scopusauthoridTsai, SN=8707094300en_HK
dc.identifier.scopusauthoridWong, RNS=7402126957en_HK

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